Concluding Remarks

The complex picture that emerges from the studies outlined above defies a simple explanation and indicates, instead, that caveolin-1 plays different roles in early -versus advanced-stage cancer cells. The growth-inhibitory actions of caveolin-1 are well established, and involve direct inhibition of mitogenic signaling pathways. It is likely that, during the early phase of cancer progression, caveolin-1 is down-regulated in order to suppress its growth-inhibitory actions and to allow rapid proliferation and clonal expansion.

Yet, it is clearly evident that caveolin-1 also exhibits pro-survival actions. We believe that these actions explain why the expression of caveolin-1 is often up-regulated at late, advanced stages of cancer, when tumor cell survival and stress resistance are of paramount importance. Although the PI3K/Akt pathway has been revealed as a major survival pathway targeted by caveolin-1, other pathways may also participate in mediating survival of malignant cells during advanced stages of cancer progression. The molecular mechanisms utilized by caveolin-1 to modulate the activity of these pathways have still to be fully elucidated. Likewise, an intriguing question - the answer to which remains obscure - is how advanced stage cancer cells manage to circumvent the anti-proliferative actions of caveolin-1.

The ability of caveolin-1 to effect both growth-inhibitory and survival-promoting activities provides a rational explanation for the divergent changes of caveolin-1 expression in different cancer cells and tumor specimens, and revises the currently dominant view of caveolin-1 as a primarily tumor-suppressor-like protein. Furthermore, the context-dependent dual functionality of caveolin-1 highlights the potential of multifunctional adaptor proteins to affect cancer cell phenotype in an unpredictable manner, thus underscoring the complexity of cancer cell biology.

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